The diagnosed incidence of small intestine neuroendocrine tumors (SI-NETs) is increasing, and the underlying genomic mechanisms have not been defined for these tumors. Using exome/genome sequence analysis of SI-NETs, we identified recurrent somatic mutations and deletions in CDKN1B, the cyclin-dependent kinase inhibitor gene, which encodes p27. We observed frameshift mutations of CDKN1B in 14 of 180 SI-NETs, and we detected hemizygous deletions encompassing CDKN1B in 7 out of 50 SI-NETs, nominating p27 as a tumor suppressor and implicating cell cycle dysregulation in the etiology of SI-NET.
Although periventricular white matter injury (PWMI) is the leading cause of chronic neurological disability and cerebral palsy in survivors of premature birth, the cellular-molecular mechanisms by which ischemia-reperfusion contributes to the pathogenesis of PWMI are not well defined. To define pathophysiologic relationships among ischemia, acute cerebral white matter damage, and vulnerable target populations, we used a global cerebral ischemia-reperfusion model in the instrumented 0.65 gestation fetal sheep. We developed a novel method to make repeated measurements of cerebral blood flow using fluorescently labeled microspheres to resolve the spatial heterogeneity of flow in situ in three-dimensional space. Basal flow in the periventricular white matter (PVWM) was significantly lower than in the cerebral cortex. During global cerebral ischemia induced by carotid occlusion, flow to all regions was reduced by nearly 90%. Ischemia of 30 or 37 min duration generated selective graded injury to frontal and parietal PVWM, two regions of predilection for human PWMI. Injury was proportional to the duration of ischemia and increased markedly with 45 min of ischemia to extensively damage cortical and subcortical gray matter. Surprisingly, the distribution of PVWM damage was not uniform and not explained by heterogeneity in the degree of white matter ischemia. Rather, the extent of white matter damage coincided with the presence of a susceptible population of late oligodendrocyte progenitors. These data support that although ischemia is necessary to generate PWMI, the presence of susceptible populations of oligodendrocyte progenitors underlies regional predilection to injury.
A new class of photoswitchable axially chiral dopants with high helical twisting power was synthesized. Their reversible photoresponsive properties were well demonstrated. These materials are found suitable for dopants in chiral nematic materials for applications in novel optically addressed displays, i.e., photodisplay. Optically addressed images were demonstrated. The dopants were sufficiently responsive to an addressing light source such that a high-resolution image with gray scale could be imaged in a few seconds of irradiation time. It was further found that an image could be retained on the screen at room temperature for 24 h before being thermally erased. The high solubility of these materials in a nematic host is also of commercial interest for stability in display applications. It is worth noting here that the photodisplay device can display a high-resolution image without the need of attached drive and control electronics, substantially reducing the cost of the display unit for use in applications where paper is currently used. Their high twisting power and large solubility in common nematic liquid crystal host can facilitate small amounts of doping to induce mesophase chirality and magnify the photocontrol effect.
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